Neuroplasticity and Neuro Rehab Flashcards

1
Q

what are ways the CNS can be damaged (7)

A

trauma
metabolic disturbances
toxicity
infection
ischemia and infarction
hemorrhage
dz

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is the cellular cascade initiated by CNS lesions

A
  1. K+ exits; Na, Cl, Ca enter
  2. H2O follows Na into cells = edema
  3. glutamate & aspartate released
  4. enzyme disturbances follow & free radicals, lipases released
  5. cell membranes, genetic material in cells are damaged and die w/i 5-10min if O2 & glucose supply not restored
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are glutamate and aspartate and what is their role

A

cytotoxic
causes additional cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

how does a TIA fit in w cascade of cellular changes seen after CNS lesions

A

TIA = stoppage of flow, had deficits and then flow resumed
- stoppage so long that level of cell death was accelerated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

how does CNS “shock” present in the acute stages (5)

A

altered LOC
hypotonia
motor and sensory changes
cognitive deficits
decline in function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the pathophys behind CNS “shock” in acute stages

A

absence or slowing of neuron firing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the ischemic zone or core of a CNS lesion

A

directly damaged

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the penumbra of a CNS lesion

A

area adjacent to ischemic core
- outer rim

can be damaged also
dec activity and availability of certain enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the diaschisis

A

reduced activity in other parts of the CNS d/t loss of connectivity and communication w lesioned area(s)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the time line of the existence of CNS shock

A

lasts 5ish days
- get tone afterward

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is the goal of medical management when recovering from a CNS lesion

A

restore blood flow to ischemic core and penumbra as quickly as possible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how is blood flow restored to tissue in the penumbra and what is the significance of this

A

collateral circulation

collateral flow can only meet energy demands for several hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are 2 important considerations when medically managing a CNS lesion

A

edema has to be managed
ICP regulated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

how can the ICP be regulated

A

meds (TPA)
craniectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what specifically allows for the recovery of CNS lesions

A

neuroplasticity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

why can recovery occur spontaneously

A

edema subsides
metabolic pathways restored

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what does the evidence show for PT when recovering from CNS lesions

A

PT can inc rate and degree of recovery and neuroplastic changes
- want to be aggressive in acute/intense phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

neuroplasticity

A

ability of nervous system to respond to intrinsic or extrinsic stimuli by reorganizing its structure, function, and neuronal connections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are two processes that allow for neuroplasticity in the presence of CNS lesions

A
  1. neural connections vary in response to environment/stimuli, activity, demands, cellular environment
  2. cellular mechanism for brain to encode learning and recover from lesions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what should be avoided while healing

A

sugars/salts - dec metabolic healing
stressful environments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

when is neuroplasticity greatest

A

greatest rate in fetal stage to 2yo
- capability declines w aging but still possible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

would there be lasting deficits from a childhood trauma

A

prob not functionally
may present cognitively

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what are methods of imaging for assessing neuroplasticity

A

fMRI
SPECT
PET

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is neurogenesis

A

formation of new neurons throughout lifespan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
how does neurogenesis change w age
fairly limited in adult mammals
26
where is neurogenesis more prominent
dentate gyrus of hippocampus
27
what happens in the hippocampus
learning and memory process
28
what is synaptic uncovering
chemically induced activity in previously inactive synapses recruitment of formerly "silent" synapses
29
what is synaptogenesis
formation of new synaptic connections via axonal sprouting
30
reactive vs regenerative synaptogenesis
reactive - from nearby, healthy axons regenerative - damaged axon
31
what is the goal of cortical remapping
functional substitution
32
what is cortical remapping
intact regions of the cortex assume the function of damaged areas
33
how can cortical remapping be assessed on imaging
fMRI - what part of the brain lights up to complete a task (how was it restructured)
34
what are 4 mechanisms of neuroplasticity
neurogenesis synaptic uncovering synaptogenesis cortical remapping
35
what is BDNF
brain derived neurotrophic factor highly abundant neurotrophin in mammal brains
36
what is BDNF a key protein for
neuroplasticity processes - helps to aid in neuroplasticity
37
what can impact BDNF levels and activity
physical activity inc levels genetic polymorphisms affect BDNF activity and neuroplastic potential
38
spontaneous recovery mechanisms are limited to what? what is the impact of this?
10 wks after stroke - inflammation reduced and metabolic pathways restored this is where the 3hrs a day model is from - high levels of intense and meaningful rehab
39
how can plasticity be harmful
reliance on unaffected side associated w neuroplastic changes may limit engagement of impaired side and results in learned non-use
40
what is neurorehabilitation
goal based motor training for recovery of impaired or lost motor function
41
since healing happens whether we do anything or not, what do we want to do w our interventions
want restructuring to be helpful, not harmful - ms properly aligned, good blood flow to cells in the area
42
what is the goal of neurorehab when it comes to fostering recovery
foster recovery via neuroplasticity whenever possible
43
what cases do you see better potential for neuro rehab in
focal, stable lesions early stages of some progressive conditions
44
recovery via neuroplasticity requires active participation in: (3)
1. goal directed, challenging activities 2. age appropriate and salient activities to inc motivation 3. repetition is key
45
what is difficult ab neuro rehab
no protocols exist and limited agreement - makes prescription and dosing a challenge ex: even the typical 3hrs might not be sufficient
46
acute vs chronic phase of CNS lesion
acute - steep recovery curve in 3-6mo period chronic - after 6mo
47
how does the rate of recovery change in acute vs chronic stages
rate of recovery slows in chronic phase - still possible
48
if there has been a period of semi-automatic recovery, what does this mean for neuroplasticity
can still be induced after this period
49
what are 6 additional considerations for neuroplasticity
age nature of lesion co-morbidities PLOF cognition, motivation, mood genetic factors
50
what does age mean for neuroplasticity
younger is better
51
how can the nature of the lesion impact neuroplasticity
focal vs global - focal is one point (better) - global - everywhere, harder to nail down stable vs progressive - stable - TBI/stroke (better) - progressive - evolving, ie MS
52
what are comorbidities to consider for neuroplasticity? why are these relevant?
BMI cardiac/respiratory hx harder to push them for acute intense therapy
53
what about PLOF should be considered for neuroplasticity
fitness activity level degree of interconnections established
54
how can CNS lesion impact motivation
poor motivation - where injury is can cause depression - having brain injury itself can be hard to cope w good motivation in unsafe context - people might not realize have a brain injury
55
why genetic factors should be considered for neuroplasticity
how are they going to heal how well will they heal
56
what are components/strategies of neurorehab that promote neuroplastic changes
applied motor learning principles - practice schedules - feedback - environment prevent learned non-use - CIMT use of tech - VR, robotics - motor imagery
57
what role does environment paly in creating neuroplastic changes
more challenging vs easier environments - d/t noise, dynamic, business
58
what is CIMT
constraint induced movement therapy forced used of involved limb - uninvolved limb is constrained via sling, oven mit, etc. and involved limb engaged in challenging and meaningful tasks
59
evidence for CIMT and recovery
strong
60
who is CIMT appropriate for
people w weakness in involved and not complete paralysis
61
what can BWSTT be combined w in training
VR or robotics
62
what is BWSTT
body weight support treadmill training allows PT to facilitate normal gait pattern safely, more steps per session, improved body mechanics but may require more staff
63
research and BWSTT?
effective but no more so than overground training
64
what can robotic neurorehab devices be used for specifically
training tool and mechanism
65
evidence for robotic neurorehab devides
good evidence but costly and not widely available - requires specialized training of PT
66
what systems does VR tap into
emotional and motivational systems
67
what is VR and how is it applied in therapy
virtual reality immersive, 3D, computer-generated environment interact w or manipulate objects in virtual setting, thereby creating a safe and controlled milieu for therapy sessions
68
what population has VR been especially effective in?
peds
69
how is VR effective for neurorehab
inc motivation and compliance which promotes neuroplasticity and recovery thru inc reps of activities
70
why has there been an inc use of VR in neurorehab
recent dec in cost for systemes emergence of commercially available serious games
71
what is rTMS
repetitive transcranial magnetic stim rTMS to motor cortex can inc excitability of affected hemisphere and inhibit unaffected hemisphere to promote balance and functional reorganization
72
how does neuroplasticity change over stages of injury as evidenced by TMS mapping of corticospinal system
different neuroplastic mechanisms may occur at different stages
73
how does rTMS work
magnet placed over area of damage or the opposite side (depending on communication) - depression on active side - active side no longer inhibiting actions on other side of brain - other side of brain can continue inhibiting the active side and further depresses it
74
where can FES be used
long term to compensate for motor loss, inc safety and independence - ie lack of DF in gait
75
literature and FES
varied findings for recovery
76
what is required for motor imagery to work
intact cognition
77
what is a pro of motor imagery
free no special training
78
what does motor imagery activate
same motor pathways as physical movement similar physiological responses to overt movement
79
why do you always want to do motor imagery
every time you think ab doing the action, the neuronal pathway is trying to push thru to the ms and do it - eventually "plow thru snow pile" and will activate ms (hopefully)
80
what is regen med and rehab
interprofessional field of research and clinical practice for repair, replacement or regen of cells, tissues, and/or organs in order to restore function lost due to dz or damage
81
what has led to a rapid proliferation of research in regen med and rehab
recent advances in stem cell and tissue engineering tech
82
what are limitations to regen med
survival and appropriate differentiation of implanted cells as well as limiting proliferation
83
who is a good candidate for regen med and stem cell implantation
stable (not too much inflammation or bleeding) correct genetic programming to convert available STEM cell into cell it needs to be - don't want to let it proliferate too much
84
what is regen med looking for in pts
if there is additional STEM cells or nerves to regen
85
regen med: studies show greater recovery in who
greater recovery w combination of stem cell plus rehab rather than either approach used in isolation in animal model studies
86
pt w too much inflammation and bleeding means what for rehab
focus on stabilizing them medically than PT rehab
87
what instances in pts are you thinking that recovery isn't possible
global deficits dec level of arousal and awareness advanced, progressive dz or neurodegenerative process
88
if recovery isn't possible, what does this mean for rehab
look for ways to compensate or substitute
89
compensation vs substitution
compensation - use of AD, w/c, AFO to mobilize substitution - can't do motion you want, but use other ms to create different movement to reach the same goal
90
what are examples of substitutions
tenodesis grasp (often in SCI) - use automatic finger flex when extend wrist to pick something up circumduction in swing phase of gait d/t loss of rectus fem